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@ARTICLE{Xie:163955,
      author       = {N. Xie and L. Zhang and W. Gao and C. Huang and P. E.
                      Huber$^*$ and X. Zhou and C. Li and G. Shen and B. Zou$^*$},
      title        = {{NAD}+ metabolism: pathophysiologic mechanisms and
                      therapeutic potential.},
      journal      = {Signal transduction and targeted therapy},
      volume       = {5},
      number       = {1},
      issn         = {2059-3635},
      address      = {London},
      publisher    = {Macmillan Publishers, part of Springer Nature},
      reportid     = {DKFZ-2020-02168},
      pages        = {227},
      year         = {2020},
      note         = {#LA:E055#},
      abstract     = {Nicotinamide adenine dinucleotide (NAD+) and its
                      metabolites function as critical regulators to maintain
                      physiologic processes, enabling the plastic cells to adapt
                      to environmental changes including nutrient perturbation,
                      genotoxic factors, circadian disorder, infection,
                      inflammation and xenobiotics. These effects are mainly
                      achieved by the driving effect of NAD+ on metabolic pathways
                      as enzyme cofactors transferring hydrogen in
                      oxidation-reduction reactions. Besides, multiple
                      NAD+-dependent enzymes are involved in physiology either by
                      post-synthesis chemical modification of DNA, RNA and
                      proteins, or releasing second messenger cyclic ADP-ribose
                      (cADPR) and NAADP+. Prolonged disequilibrium of NAD+
                      metabolism disturbs the physiological functions, resulting
                      in diseases including metabolic diseases, cancer, aging and
                      neurodegeneration disorder. In this review, we summarize
                      recent advances in our understanding of the molecular
                      mechanisms of NAD+-regulated physiological responses to
                      stresses, the contribution of NAD+ deficiency to various
                      diseases via manipulating cellular communication networks
                      and the potential new avenues for therapeutic intervention.},
      subtyp        = {Review Article},
      cin          = {E055},
      ddc          = {610},
      cid          = {I:(DE-He78)E055-20160331},
      pnm          = {315 - Imaging and radiooncology (POF3-315)},
      pid          = {G:(DE-HGF)POF3-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33028824},
      pmc          = {pmc:PMC7539288},
      doi          = {10.1038/s41392-020-00311-7},
      url          = {https://inrepo02.dkfz.de/record/163955},
}